Collagen Arthritis in T Cell Receptor Congenic Mice

Nabozny, Gerald H.; David, Chella S.

doi:10.1007/978-1-4615-1891-4_12

Cited by 3 publications

(3 citation statements)

References 18 publications

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“…In similarity with the situation in EAE, many TCR V genes are used for recognition of CII, although a more restricted response could possibly occur at the peptide level (Osman et al 1993, Corthay et al, manuscript in preparation). Genetic analyses have not shown any conclusive evidence for the importance of TCR polymorphism (Andersson et al 1991, Banerjee et al 1988, Nabozny et al 1994, Spinella et al 1991 in contrast to previous postulates (Anderson et al 1991, Banerjee et al 1988.…”

Section: Usage Of T-cell Receptorsmentioning

confidence: 86%

Chronicity of Tissue‐Specific Experimental Autoimmune Disease: A Role for B Cells?

Holmdahl¹,

Vingsbo²,

Mo³

et al. 1995

Immunological Reviews

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Section: Usage Of T-cell Receptorsmentioning

confidence: 86%

Chronicity of Tissue‐Specific Experimental Autoimmune Disease: A Role for B Cells?

Holmdahl¹,

Vingsbo²,

Mo³

et al. 1995

Immunological Reviews

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“…The presence of V,8 or V,6 T cells within arthritic joints has also been described in CIA (18,(39)(40)(41). Involvement of the V,8 T cell family appears to be common to a number of murinc autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE) (42)(43)(44), experimental myasthenia gravis (454, experimental thyroiditis (46), and MRL disease (47,48), as well as within the pancreatic lesion in diabetic NOD mice (49) and the salivary gland lesions in experimental SjGgren's syndrome (50).…”

Section: Discussionmentioning

confidence: 84%

Pristane-induced arthritis in mice: V. Susceptibility to pristane-induced arthritis is determined by the genetic regulation of the T cell repertoire

Wooley¹,

Sud²,

Whalen³

et al. 1998

Arthritis & Rheumatism

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Objective. Pristane-induced arthritis (PIA) is an experimental seropositive arthritis that is characterized by serologic and cellular immune abnormalities and is dependent on the presence of a competent CD4+ T cell population. We examined the regulation of PIA by genes of the major histocompatibility complex (MHC) and the Mls-1 loci to determine whether the selection of' the T cells that infiltrate arthritic joints is a critical factor in disease susceptibility.Methods. Genetic regulation of PIA was investigated using F, hybrid and congenic strain analysis to determine the influence of MHC and Mls-1 genes. The T cell receptor V, phenotypes of lymph node cells and T cells infiltrating arthritic joints were examined with 2-color flow cytometry and reverse transcriptionpolymerase chain reaction techniques.Results. F, hybrid offspring from 2 major PIAsusceptible strains (DBN1 x BALBlc) were resistant to the induction of arthritis because of the interaction between genes of the MHC and the Mls-I loci, which modified the T cell repertoire. This conclusion was supported by the observed resistance to PIA in BALB/ c-Mls-I" mice, where T cells expressing the V,8.1 and V,6 phenotypes were absent. The receptor phenotype of T cells infiltrating arthritic joints in DBN1 mice was markedly skewed toward V,8.

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“…Studies of the TCR repertoire expressed in the lymph nodes and joints of mice with CIA have suggested that there are a few Va and V p genes that arc preferentially used (12,13). Furthermore, injection of some anti-Vp monoclonal antibodies (MAb) can modulate the development of CIA (13)(14)(15). The hypothesis that T cells expressing particular V p chains influence CIA development was extensively tested (9,(16)(17)(18)(19)(20).…”

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confidence: 99%

Genetic control of susceptibility to collagen-induced arthritis in T cell receptor ?-chain transgenic mice

Mori

Libero

1998

Arthritis & Rheumatism

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Objective. To study the genes in the mouse background which predispose to the development of collagen-induced arthritis (CIA). Methods. T cell receptor P transgenic (TCRPL)mice that have a T cell repertoire that predisposes to the development of CIA were used. Classic genetic studies and microsatellite gene mapping were done in (SWR-PL X DBA/l)F, hybrid mice.Results. Besides TCRP, major histocompatibility complex class 11, and Igh-C, at least 2 other genes are absolutely required for CIA development in these mice. A strict association of CIA with the presence of functional complement C5 allele (Hc') was found, suggesting that Hc' or a closely linked gene might be one of these essential genes.Conclusion. This study provides new evidence of the pathogenetic role of complement C5 in CIA. Furthermore, these transgenic mice may facilitate molecular identification of other genes that predispose to CIA.Collagen-induced arthritis (CIA) is a chronic inflammatory arthropathy considered to be an experimental model of rheumatoid arthritis (RA). CIA develops in mice, rats, and primates after immunization with native type I1 collagen (CII) in adjuvant (1-3). Although the precise mechanisms by which CIA develops arc not known, several findings indicate that the disease is due to autoreactivity to CII (for review, see ref. 4). Both cellular and T cell-dependent humoral anti-CII immune responses are important for the pathogenesis of the Supported by Swiss National Science Foundation grants .

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Collagen Arthritis in T Cell Receptor Congenic Mice

Cited by 3 publications

References 18 publications

Chronicity of Tissue‐Specific Experimental Autoimmune Disease: A Role for B Cells?

Chronicity of Tissue‐Specific Experimental Autoimmune Disease: A Role for B Cells?

Pristane-induced arthritis in mice: V. Susceptibility to pristane-induced arthritis is determined by the genetic regulation of the T cell repertoire

Genetic control of susceptibility to collagen-induced arthritis in T cell receptor ?-chain transgenic mice

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